The importance of inflammatory mechanisms in alzheimer disease

The importance of inflammatory mechanisms in alzheimer disease Lesions in such chronic neurodegenerative disorders as Alzheimer disease (AD), Parkinson disease, the parkinsonism dementia complex of Guam, and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. This is particularly true of AD, where inflammatory reactions are thought to be important contributors to the neuronal loss. Proteins present include complement proteins, complement inhibitors, acute phase reactants, inflammatory cytokines, proteases, and protease inhibitors. Studies of cultured human astrocytes and microglia, obtained from postmortem brain, have established that nearly all of these proteins are produced by one or another of these cell types. Human neurons also produce many inflammatory proteins and their inhibitors, creating complex interactions. Accumulations of amyloid and extracellular tangles apparently act as irritants, causing the activation of complement, the initiation of reactive changes in microglia, and the release of potentially neurotoxic products. Such products include the membrane attack complex, oxygen free radicals, and excess glutamate. Twenty epidemiological studies that have been published to date indicate that populations taking antiinflammatory drugs have a significantly reduced prevalence of AD or a slower mental decline. One small clinical trial with indomethacin showed arrest of the disease over a six-month period. Therapeutic intervention in key inflammatory processes holds great promise for the amelioration of AD and possibly other neurodegenerative disorders. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Gerontology Elsevier

The importance of inflammatory mechanisms in alzheimer disease

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Publisher
Elsevier
Copyright
Copyright © 1998 Elsevier Science Inc.
ISSN
0531-5565
eISSN
1873-6815
D.O.I.
10.1016/S0531-5565(98)00013-8
Publisher site
See Article on Publisher Site

Abstract

Lesions in such chronic neurodegenerative disorders as Alzheimer disease (AD), Parkinson disease, the parkinsonism dementia complex of Guam, and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. This is particularly true of AD, where inflammatory reactions are thought to be important contributors to the neuronal loss. Proteins present include complement proteins, complement inhibitors, acute phase reactants, inflammatory cytokines, proteases, and protease inhibitors. Studies of cultured human astrocytes and microglia, obtained from postmortem brain, have established that nearly all of these proteins are produced by one or another of these cell types. Human neurons also produce many inflammatory proteins and their inhibitors, creating complex interactions. Accumulations of amyloid and extracellular tangles apparently act as irritants, causing the activation of complement, the initiation of reactive changes in microglia, and the release of potentially neurotoxic products. Such products include the membrane attack complex, oxygen free radicals, and excess glutamate. Twenty epidemiological studies that have been published to date indicate that populations taking antiinflammatory drugs have a significantly reduced prevalence of AD or a slower mental decline. One small clinical trial with indomethacin showed arrest of the disease over a six-month period. Therapeutic intervention in key inflammatory processes holds great promise for the amelioration of AD and possibly other neurodegenerative disorders.

Journal

Experimental GerontologyElsevier

Published: Aug 1, 1998

References

  • The role of the immune system in neurodegenerative disorders
    McGeer, E.G.; McGeer, P.L.
  • The inflammatory system of brain
    McGeer, P.L.; McGeer, E.G.
  • Neuronal expression of mRNAs for complement proteins of the classical pathway in Alzheimer brain
    Shen, Y.; Li, R.; McGeer, E.G.; McGeer, P.L.
  • Neurons express proteins of the classical complement pathway in Alzheimer disease
    Terai, K.; McGeer, E.G.; McGeer, P.L.

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